Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Circadian Clock- and Transcription-controlled Genome-wide Excision Repair of UV Damage in Arabidopsis

ABSTRACT: Circadian Clock- and Transcription-controlled Genome-wide Excision Repair of UV Damage in Arabidopsis

PROVIDER: PRJNA429185 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Circadian Clock- and Transcription-controlled Genome-wide Excision Repair of UV Damage in Arabidopsis

Project description:We used the recently developed Excision Repair-sequencing (XR-seq) method to study genome-wide repair of UV-induced DNA damage in Arabidopsis. We found that the repair of cyclobutane pyrimidine dimers for a large fraction of the genome is controlled by the joint actions of the circadian clock and transcription by RNA polymerase II. Arabidopsis has a relatively compact genome, and a large fraction of the genes are controlled by the circadian clock. Our data on the interface of these two global regulatory systems reveal very strong repair preference of the transcribed strands of Arabidopsis genes, 10 to 30% of which are circadian time-dependent. Thus, throughout the day, Arabidopsis exhibits enormous dynamic range in repair to cope with exposure to sunlight.

2018-04-17 | GSE108932 | GEO

Excision repair hotspots of UV-induced DNA damage in the human genome

Project description:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.

2020-04-09 | GSE148303 | GEO

Genome-wide analysis of human global and transcription-coupled excision repair of UV damage at single-nucleotide resolution

Project description:We developed a method for genome-wide mapping of DNA excision repair named XR-seq (eXcision Repair-seq). Human nucleotide excision repair generates two incisions surrounding the site of damage, creating a ~30-mer. In XR-seq, this fragment is isolated and subjected to high-throughput sequencing. We used XR-seq to produce stranded, nucleotide-resolution maps of repair of two UV-induced DNA damages in human cells, cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts ((6-4)PPs). In wild-type cells, CPD repair was highly associated with transcription, specifically with the template strand. Experiments in cells defective in either transcription-coupled excision repair or general excision repair isolated the contribution of each pathway to the overall repair pattern, and showed that transcription-coupled repair of both photoproducts occurs exclusively on the template strand. XR-seq maps capture transcription-coupled repair at sites of divergent gene promoters and bi-directional eRNA production at enhancers. XR-seq data also uncovered the repair characteristics and novel sequence preferences of CPDs and (6-4)PPs. XR-seq and the resulting repair maps will facilitate studies of the effects of genomic location, chromatin context, transcription, and replication on DNA repair in human cells. We have performed XR-seq for two types of UV-induced damages (CPD and (6-4)PP) in three different cell lines: NHF1, XP-C (XP4PA-SV-EB, GM15983)), and CS-B (CS1ANps3g2, GM16095). Two biological replicates were performed for each experiment, in which independent cell populations were UV treated and subjected to XR-seq.

2015-04-19 | E-GEOD-67941 | biostudies-arrayexpress

Circadian clock controlled gene expression in soybean seeds

2010-06-21 | GSE18827 | GEO

Circadian clock controlled gene expression in soybean seeds

Project description:Microarray expression profiling was used to identify genes expressed in developing soybean (Glycine max) seeds that are controlled by the circadian clock. Plants with developing seeds were entrained to 12hour light: 12 hour dark cycles and sampled in constant light conditions. Soybean seeds entrained to 12 hour-light:12 hour dark photocycles were harvested after 24 hours of constant light and temperature conditions. Timepoint 24h represents subjective dawn. To minimize developmental variation, flowers were marked as they opened and seeds were harvested from marked pods after 5 weeks. There are two replicate samples at each time point, and each sample consists of 8 seeds collected from three diffferent plants.

2010-07-08 | E-GEOD-18827 | biostudies-arrayexpress

Cisplatin-DNA Adduct Repair of Transcribed Genes is Controlled by Two Circadian Programs in Mouse Tissues

Project description:We tested the impact of clock time on excision repair of cisplatin-induced DNA damage at single nucleotide resolution across the genome in mouse liver and kidney. We found that genome repair is controlled by two circadian programs.

2018-06-21 | GSE109938 | GEO

TIMP3, a CLOCK-controlled gene, determines cell susceptibility to UV-induced expression of inflammatory factors in human keratinocytes.

Project description:To search for CLOCK-controlled genes in human keratinocytes, we introduced siRNAs against CLOCK and harvested the cells at two time points, ZT 32 and 44. We speculated that those genes that were downregulated at both ZT time points may be selectively regulated by CLOCK

2020-05-15 | GSE98900 | GEO

Genome-wide analysis of human global and transcription-coupled excision repair of UV damage at single-nucleotide resolution

2015-04-19 | GSE67941 | GEO

Excision repair hotspots of UV-induced DNA damage in the human genome

Project description:Excision repair hotspots of UV-induced DNA damage in the human genome

| PRJNA623860 | ENA

eXcision Repair-sequencing (XR-seq) to map UV induced damage in U2OS cells and in U2OS cells in which CSA or UVSSA genes were knocked out

Project description:We used eXcision Repair-sequencing (XR-seq) to map UV induced damage in U2OS cells and in U2OS cells in which CSA or UVSSA genes were knocked out. Complementation of UVSSA knockout with WT or mutant proteins shows UVSSA is a core component of human transcription coupled repair.

2020-04-13 | GSE132840 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data